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Hyperglycemia and cardiomyocytes

Ravichandra Shivalingappa Davargaon, Asha Devi Sambe, Subramanyam Muthangi V V
Oxidative stress (OS) has been implicated in a variety of pathological conditions, including diabetes mellitus, characterized by hyperglycemia. In the present study, OS induced by hyperglycemia and the effect of trolox, a vitamin E analog, were studied in cardiomyocytes and H9c2 cells exposed to 15 to 33 mM glucose (HG) for 24 to 72 hours in Dulbecco modified Eagle medium. Cells treated wirh 24 or 33 mM glucose for 24 hours or above showed decreased viability and adenosine triphosphate (ATP) content with a concomitant increase in radicals of oxygen species, calcium (Ca2+ ), mitochondrial permeability transition, and oxidative markers, confirming that the cells were under stress...
December 4, 2018: Journal of Biochemical and Molecular Toxicology
Aysegul Durak, Yusuf Olgar, Sinan Degirmenci, Erman Akkus, Erkan Tuncay, Belma Turan
BACKGROUND: Metabolic syndrome (MetS) is a prevalent risk factor for cardiac dysfunction. Although SGLT2-inhibitors have important cardioprotective effects in hyperglycemia, their underlying mechanisms are complex and not completely understood. Therefore, we examined mechanisms of a SGLT2-inhibitor dapagliflozin (DAPA)-related cardioprotection in overweight insulin-resistant MetS-rats comparison with insulin (INSU), behind its glucose-lowering effect. METHODS: A 28-week high-carbohydrate diet-induced MetS-rats received DAPA (5 mg/kg), INSU (0...
November 17, 2018: Cardiovascular Diabetology
Yusuf Olgar, Belma Turan
Sodium-glucose cotransporter 2 (SGLT2)-inhibitors showed significant effect in patients with diabetes or metabolic syndrome, MetS with high cardiovascular-risk. Although the increased intracellular Zn2+ level ([Zn2+]i), oxidative stress and alterated cardiac matrix metalloproteinases (MMPs) in diabetic cardiomyopathy can intersect with different signaling pathways, the exact mechanisms are not known yet. Since either MMPs or SGLT2 have important role in cardiac-fibrosis under hyperglycemia, we aimed to examine the role of SGLT2-inhibitor dapagliflozin (DAP) on cardiac Zn2+-transporters responsible from [Zn2+]i-regulation, comparison to insulin (INS), together with MMP levels and systemic oxidative-stress-status in MetS-rats...
November 16, 2018: Canadian Journal of Physiology and Pharmacology
Jakob G Knudsen, Alexander Hamilton, Reshma Ramracheya, Andrei I Tarasov, Melissa Brereton, Elizabeth Haythorne, Margarita V Chibalina, Peter Spégel, Hindrik Mulder, Quan Zhang, Frances M Ashcroft, Julie Adam, Patrik Rorsman
Diabetes is a bihormonal disorder resulting from combined insulin and glucagon secretion defects. Mice lacking fumarase (Fh1) in their β cells (Fh1βKO mice) develop progressive hyperglycemia and dysregulated glucagon secretion similar to that seen in diabetic patients (too much at high glucose and too little at low glucose). The glucagon secretion defects are corrected by low concentrations of tolbutamide and prevented by the sodium-glucose transport (SGLT) inhibitor phlorizin. These data link hyperglycemia, intracellular Na+ accumulation, and acidification to impaired mitochondrial metabolism, reduced ATP production, and dysregulated glucagon secretion...
November 1, 2018: Cell Metabolism
Jing Tian, Wenzhu Tang, Ming Xu, Chen Zhang, Pei Zhao, Tongtong Cao, Xiaoli Shan, Rong Lu, Wei Guo
BACKGROUND/AIMS: Shengmai San (SMS), prepared from Panax ginseng, Ophiopogon japonicus, and Schisandra chinensisin, has been widely used to treat ischemic disease. In this study, we investigated whether SMS may exert a beneficial effect in diabetic cardiomyopathy through improvement of mitochondrial lipid metabolism. METHODS: A leptin receptor-deficient db/db mouse model was utilized, and lean age-matched C57BLKS mice served as non-diabetic controls. Glucose and lipid profiles, myocardial structure, dimension, and function, and heart weight to tibial length ratio were determined...
2018: Cellular Physiology and Biochemistry
Gwo-Jyh Chang, Yung-Hsin Yeh, Wei-Jan Chen, Yu-Shien Ko, Jong-Hwei S Pang, Hsiao-Yu Lee
Diabetic patients with cardiomyopathy show a higher incidence of arrhythmias and sudden death. Chronic hyperglycemia induces the formation of advanced glycation end products (AGEs), which contribute to the pathogenesis of diabetic cardiomyopathy. This study investigated whether inhibition of AGEs formation by aminoguanidine (AG) could prevent the cardiac electromechanical and arrhythmogenic remodeling in diabetes mellitus. Streptozotocin-induced diabetic rats received AG (100 mg/kg daily, IP) or vehicle (normal saline, IP) for 5 weeks...
October 31, 2018: Journal of Pharmacology and Experimental Therapeutics
Weijian Hang, Benhong He, Jiehui Chen, Liangtao Xia, Bing Wen, Tao Liang, Xu Wang, Qianying Zhang, Yue Wu, Qingjie Chen, Juan Chen
Background: Type II diabetes (T2D)-induced cardiomyocyte hypertrophy is closely linked to the impairment of mitochondrial function. Berberine has been shown to be a promising effect for hypoglycemia in T2D models. High glucose-induced cardiomyocyte hypertrophy in vitro has been reported. The present study investigated the protective effect and the underlying mechanism of berberine on high glucose-induced H9C2 cell line. Methods: High glucose-induced H9C2 cell line was used to mimic the hyperglycemia resulting in cardiomyocyte hypertrophy...
2018: Frontiers in Pharmacology
Chen Zhao, Qile Shen
Hyperglycemia may induce diabetic cardiomyopathy (DC). In the current study, the mechanism underlying the alleviation of high glucose (HG)‑induced impairments in the proliferation of H9c2 embryo cardiomyocyte proliferation by small ubiquitin‑like modifier 2 (SUMO2) overexpression was investigated. H9c2 cell morphology was identified as classical long shuttle type by optical microscopy. The viability of HG‑injured H9c2 cells was evaluated by a Cell Counting Kit‑8 assay and the results indicated that viability was inhibited in a dose‑dependent (5...
December 2018: Molecular Medicine Reports
Yan-Jun Song, Chong-Bin Zhong, Xian-Bao Wang
Acute myocardial infarction is a major cause of death worldwide. The most important therapy for limiting ischemic injury and infarct size is timely and efficient myocardial reperfusion treatment, which may instead induce cardiomyocyte necrosis due to myocardial ischemia-reperfusion (I/R) injury. Heat shock protein 70 (HSP70), a stress-inducible protein, is overexpressed during myocardial I/R. The induced HSP70 is shown to regulate several intracellular proteins (e.g., transcription factors, enzymes, and apoptosis-related proteins) and signaling pathways (e...
August 21, 2018: Journal of Cellular Physiology
Belma Turan
Zinc (mostly as free/labile Zn2+ ) is an essential structural constituent of many proteins, including enzymes in cellular signaling pathways via functioning as an important signaling molecule in mammalian cells. In cardiomyocytes at resting condition, intracellular labile Zn2+ concentration ([Zn2+ ]i ) is in the nanomolar range, whereas it can increase dramatically under pathological conditions, including hyperglycemia, but the mechanisms that affect its subcellular redistribution is not clear. Therefore, overall, very little is known about the precise mechanisms controlling the intracellular distribution of labile Zn2+ , particularly via Zn2+ transporters during cardiac function under both physiological and pathophysiological conditions...
August 8, 2018: Biological Trace Element Research
Kunal Sikder, Sanket Kumar Shukla, Neel Patel, Harpreet Singh, Khadija Rafiq
BACKGROUND/AIMS: Systemic hyperlipidemia and intracellular lipid accumulation induced by chronic high fat diet (HFD) leads to enhanced fatty acid oxidation (FAO) and ketogenesis. The present study was aimed to determine whether activation of peroxisome proliferator-activated receptor-γ (PPAR-γ) by surplus free fatty acids (FA) in hyperlipidemic condition, has a positive feedback regulation over FAO and ketogenic enzymes controlling lipotoxicity and cardiac apoptosis. METHODS: 8 weeks old C57BL/6 wild type (WT) or PPAR-γ-/- mice were challenged with 16 weeks 60% HFD to induce obesity mediated type 2 diabetes mellitus (T2DM) and diabetic cardiomyopathy...
2018: Cellular Physiology and Biochemistry
Linda Alex, Ilaria Russo, Volodymir Holoborodko, Nikolaos G Frangogiannis
Heart failure with preserved ejection fraction (HFpEF) is caused, or exacerbated by, a wide range of extracardiac conditions. Diabetes, obesity, and metabolic dysfunction are associated with a unique HFpEF phenotype, characterized by inflammation, cardiac fibrosis, and microvascular dysfunction. Development of new therapies for HFpEF is hampered by the absence of reliable animal models. The leptin-resistant db/ db mouse has been extensively studied as a model of diabetes-associated cardiomyopathy; however, data on the functional and morphological alterations in db/ db hearts are conflicting...
October 1, 2018: American Journal of Physiology. Heart and Circulatory Physiology
Woong Bi Jang, Ji Hye Park, Seung Taek Ji, Na Kyung Lee, Da Yeon Kim, Yeon Ju Kim, Seok Yun Jung, Songhwa Kang, Shreekrishna Lamichane, Babita Dahal Lamichane, Jongseong Ha, Jisoo Yun, Hyung Ryong Moon, Sang Hong Baek, Hae Young Chung, Sang-Mo Kwon
Diabetic cardiomyopathy (DCM) is tightly linked to heart disorders and dysfunction or death of the cardiomyocytes including resident cardiac progenitor cells (CPCs) in diabetic patients. In order to restore loss of function of resident or transplanted CPCs, much research has focused on novel therapeutic strategies including the discovery of novel function-modulating factors such as reactive oxygen species (ROS) scavengers. Here, we developed and defined a novel antioxidant, MHY-1684, for enhancing the angiogenic potential of CPCs against ROS-related DCM...
2018: Oxidative Medicine and Cellular Longevity
Lorna J Daniels, Rachel S Wallace, Olivia M Nicholson, Genevieve A Wilson, Fiona J McDonald, Peter P Jones, J Chris Baldi, Regis R Lamberts, Jeffrey R Erickson
BACKGROUND: Calcium/calmodulin-dependent kinase II-delta (CaMKIIδ) activity is enhanced during hyperglycemia and has been shown to alter intracellular calcium handling in cardiomyocytes, ultimately leading to reduced cardiac performance. However, the effects of CaMKIIδ on cardiac contractility during type 2 diabetes are undefined. METHODS: We examined the expression and activation of CaMKIIδ in right atrial appendages from non-diabetic and type 2 diabetic patients (n = 7 patients per group) with preserved ejection fraction, and also in right ventricular tissue from Zucker Diabetic Fatty rats (ZDF) (n = 5-10 animals per group) during early diabetic cardiac dysfunction, using immunoblot...
June 14, 2018: Cardiovascular Diabetology
Miao Guo, Hong-Xia Wang, Wen-Jun Chen
Diabetic cardiomyopathy is a cascade of complex events leading to eventual heart failure in diabetes. JQ1, one of Bromodomain and extra-terminal domain (BET) protein inhibitors, has exerted therapeutic effects on cancer proliferation, inflammation and cardiovascular disease. Recently, JQ1 was reported to protect mice from bleomycin-induced lung fibrosis and reverse the fibrotic response in carbon tetrachloride-induced liver fibrosis. However, its role in diabetic cardiomyopathy remains to be clarified. Our results indicated that JQ1 treatment suppressed cardiac fibrosis and improved cardiac function in a STZ-induced diabetic mouse model...
August 1, 2018: Toxicology and Applied Pharmacology
Nur Liyana Mohammed Yusof, Satirah Zainalabidin, Norsyahida Mohd Fauzi, Siti Balkis Budin
Diabetes mellitus is often associated with cardiac functional and structural alteration, an initial event leading to cardiovascular complications. Roselle (Hibiscus sabdariffa) has been widely proven as an antioxidant and recently has incited research interest for its potential in treating cardiovascular disease. Therefore, this study aimed to determine the cardioprotective effects of H. sabdariffa (roselle) polyphenol-rich extract (HPE) in type-1-induced diabetic rats. Twenty-four male Sprague-Dawley rats were randomized into 4 groups (n = 6/group): nondiabetic, diabetic alone (DM), diabetic supplemented with HPE (DM+HPE), and diabetic supplemented with metformin...
May 4, 2018: Applied Physiology, Nutrition, and Metabolism, Physiologie Appliquée, Nutrition et Métabolisme
Jun Hou, Dezhi Zheng, Wenjing Xiao, Dandan Li, Jie Ma, Yonghe Hu
Mangiferin functions as a perfect anti-oxidative compound in the diabetic heart, however, the exact mechanism remains to be elucidated. Here, we show the cardioprotective effect of mangiferin under high glucose-induced cardiotoxic condition mainly contributed to enhanced autophagy via suppressing mTORC1 downstream signal transduction. Primary neonatal rat cardiomyocytes were cultured to detect myocytes injury, autophagy, and related signal transduction under different doses of glucose and mangiferin treatment...
2018: Frontiers in Pharmacology
Soni Deshwal, Marleen Forkink, Chou-Hui Hu, Guido Buonincontri, Salvatore Antonucci, Moises Di Sante, Michael P Murphy, Nazareno Paolocci, Daria Mochly-Rosen, Thomas Krieg, Fabio Di Lisa, Nina Kaludercic
Monoamine oxidase (MAO) inhibitors ameliorate contractile function in diabetic animals, but the mechanisms remain unknown. Equally elusive is the interplay between the cardiomyocyte alterations induced by hyperglycemia and the accompanying inflammation. Here we show that exposure of primary cardiomyocytes to high glucose and pro-inflammatory stimuli leads to MAO-dependent increase in reactive oxygen species that causes permeability transition pore opening and mitochondrial dysfunction. These events occur upstream of endoplasmic reticulum (ER) stress and are abolished by the MAO inhibitor pargyline, highlighting the role of these flavoenzymes in the ER/mitochondria cross-talk...
September 2018: Cell Death and Differentiation
Rebecca Sullivan, Rebecca McGirr, Shirley Hu, Alice Tan, Derek Wu, Carlie Charron, Tyler Lalonde, Edith Arany, Subrata Chakrabarti, Leonard Luyt, Savita Dhanvantari
Ghrelin and its receptor, the growth hormone secretagogue receptor 1a (GHSR1a), are present in cardiac tissue. Activation of GHSR1a by ghrelin promotes cardiomyocyte contractility and survival, and changes in myocardial GHSR1a and circulating ghrelin track with end-stage heart failure, leading to the hypothesis that GHSR1a is a biomarker for heart failure. We hypothesized that GHSR1a could also be a biomarker for diabetic cardiomyopathy (DCM). We used two models of streptozotocin (STZ)-induced DCM: group 1, adult mice treated with 35 mg/kg STZ for 3 days; and group 2, neonatal mice treated with 70 mg/kg STZ at days 2 and 5 after birth...
February 1, 2018: Journal of the Endocrine Society
Wei Sheng Tan, Thomas P Mullins, Melanie Flint, Sarah L Walton, Helle Bielefeldt-Ohmann, David A Carter, Meera R Gandhi, Hayley R McDonald, Joan Li, Karen M Moritz, Melissa E Reichelt, Linda A Gallo
There is an increased incidence of heart failure in individuals with diabetes mellitus (DM). The coexistence of kidney disease in DM exacerbates the cardiovascular prognosis. Researchers have attempted to combine the critical features of heart failure, using transverse aortic constriction, with DM in mice, but variable findings have been reported. Furthermore, kidney outcomes have not been assessed in this setting; thus its utility as a model of heart failure in DM and kidney disease is unknown. We generated a mouse model of obesity, hyperglycemia, and mild kidney pathology by feeding male C57BL/6J mice a high-fat diet (HFD)...
June 1, 2018: American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
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